U world 5/16
Terms in this set (66)
Mediators of systemic inflammatory response, stimulate secretion of acute-phase proteins
IL-1, IL-6, TNF-a
Staus epilepticus treatment
Benzodiazepines are 1st line + Phenytoin to prevent recurrence
inhibits neuronal high-frequency firing by reducing ability of Na channels to recover from inactivation
5-HT 1B/1D agonists, affect post synaptic serotonin receptor stimulation. Inhibit relase vasoactive peptides, promote vasoconstriction, block pain pathways
DA NE reuptake inhibitor
Presynaptic 5HT and NE reuptake inhibition
How do non selective B blockers cause problems in diabetics?
Inhibit EPI and NE mediated compensatory rxn to hypoglycemia + Inhibit hepatic gluconeogenesis and pheripheral glycogenolysis and lipolysis
Neuroleptic malignant syndrome
hyperthermia, extreme generalized rigidity, autonomic instability, altered mental status
hepatic failure: microvesicular steatosis; swelling decreased number mitochondria; glycogen depletion
Encephalopathy: toxic effect of hyperammonemia on CNS
Viral hepatitis liver findings
injury: ballooning degeneration
death: lobular architecture disruption and hepatocyte necrosis
Htn; basal ganglia, cerebellum, thalamus, pons; intracerebral hemorrhage ; progressive neuro deficit, headache may follow
ADPKD, Ehlers Danlos, htn; circle of willis; subarachnoid hemorrhage
MOA SGLT2 inhibitors
Canagliflozin, dapagliflozin. Decrease proximal tubular resorption of glucose; promote urinary glucose loss. *Monitor creatinine
fallopian tube epithelium
simple pseudostratified columnar
simple columnar (endo), Stratified squamous (ecto)
stratified squamous non-keratinized
MOA diabetic neuropathy
Non-enz glycosylation=microangiopathy of endoneural arterioles and ischemic nerve damage
Osmotic damage to axons and schwann cells (via aldose reductase)
cystic tumor in cerebellum of child
Histology of pilocytic astrocytoma
well-diff neoplasm comprised of spindle cells with hair-ike glial processes associated with microcyts + rosenthal fibers and granular eosino bodies
Findings post MI
2 weeks- 2 mo
1. minimal change
2. early coag necrosis, edema, hemorrhage, wavy fibers
3. coag necrosis, marginal contraction, band necrosis
4. + inflamm infiltrate
5. macrohpage phagocytosis
6. granulation tissue and neovasculariztion
7. collagen deposition/scar
How long does it take to a scar to form post-MI?
2 weeks to 2 months
Why add carbidopa to levodopa?
Reduce most of peripheral side fx of levodopa
What is a side effect of adding levodopa to carbidopa?
Behavioral changes from levodopa worsen because more DA available to brain
Acute neonatal narcotic withdrawal presentation
pupillary dilation, rhinorrhea, sneezing, nasal stuffiness, diarrhea, nausea, vomiting, chills, tremor, jitters, may lead to seizures
How do you treat acute neonatal narcotic withdrawal?
Parathyroid, pancreatic tumor, pituitary adenoma
Medullary carcinoma of thyroid, pheochromocytoma, parathyroid
Medullary carcinoma of thyroid, pheo, marfanoid, mucosal neuromas
Nicotinic receptor and neurotransmitter?
Ligand-gated, open after binding ACh; Influx of Na, Ca into cell, K out of cel
Squamous cell carcinoma of esophagus
Chronic alcohol abuse + smoking. Will see foci of keratinization in well-differentiated tumors
Solid sheets of small cells with dark nuclei and scant cytoplasm
middle meningeal artery
cortical bridging beins
rupture of berry aneurysm
lateral striate arteries from MCA
What type of diverticular are colonic diverticula?
HLA-B27 spondyloarthropathy following infection by chlamydia, campy, salmonella, shigella, yersinia
Neurosyphillis; degeneration of dorsal columns and dorsal roots of spinal cord
Tabes dorsalis symptoms
loss of proprioception, vibration. Ataxia, Argyll Robertson pupil
TZD side effects
fluid retention, weight gain, edemam
factors increasing/decreasing renal stones
Increased in: high concentration Ca, PO4, Oxalate, Uric acid
Decreased: increased citrate and high fluid intake
Require acidic pH for formation of some crystals
Maternal diabetes affect on fetus
Caudal regression syndrome, congenital heart defects, neural tube defects
CFTR 3 base pair deletion removes phenylalanine at 508. Impaired posttranslational processing...abnormal protein can't reach cell surface
Hyper IgM syndrome
inability of B-lymphocytes to undergo isotype switching. Lymphoid hyperplasia + recurrent sinopulmonary infections
Cause of hyper IgM?
genetic absence of CD-40L on T cells or from genetic def in enzymes responsibile for isotype switching
what contributes to HCV variability?
Lack of proofreading 3'-5' exonuclease activity
Most common cause of fetal hydronephrosis?
Inadequate recanalization of ureteropelvic junction between kidney and ureter. This is the last segment to canalize, and thus the most likely site for obsturction
Comorbidities of Diabetes Mellitus....what is leading cause of death?
Cardiovascular disease, though DM is the leading cause of ESRD, of those with ESRD 50% die due to cardiovascular disease
Most common finding of PCA stroke?
contralateral homonymous hemianopia, often with macular sparing
TSH stimulates thyroid to produce?
T4, T4 is then converted peripherally to T3 and rT3
Angiogenesis is driven by?
Hyperosmotic volume contraction
Loss of free water exceeds loss ofelectrolytes = increased osmolarity and contracted volumes in ICF, ECF
Causes of diabetes insipidius
Acute GI hemorrhage findings
Isotonic loss of ECF volume, isosmotic volume contraction. No effect on osmolarity or icf
Hypertonic loss of NaCl. Low osmolarity of ECF shifts free water into ICF causing ICF expansion
Hypertonic saline infusion
Hypertonic volume expansion...shefts water from ICF to ECF
Primary polydipsia and SIADH
Expansion of ECF and ICF, decrease osmolarity
Night blindness, itching, dry skin
Vitamin A deficiency as a result of malabsorption due to chronic cholestasis (biliary obstruction)
Blood supply to Wernicke and Broca?
When do cilia end in the bronchial tree?
Not present in alveolar ducts or alveoli, but everywhere else
Drugs inducing lupus + findings
Rarely see anti-dsDNA
Will see: ANA and anti-histone
Mechanism of disease prevention in influenza virus
Inactivated vaccine induce neutralizing antibodies against hemagluttinin antigen. Upon exposure to virus, antibodies inhibit HA binding to sialylated receptors on host cell membrane, preveting live virus from entering cells via endocytosis
What kind of response to inactivated vaccines generate?
What kind of response do live-attenuated vaccines generate?
Strong cell-mediated immune response and humoral immunity
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